Search results for "HMG-COA REDUCTASE"

showing 10 items of 34 documents

HMG-CoA reductase promotes protein prenylation and therefore is indispensible for T-cell survival.

2017

AbstractStatins are a well-established family of drugs that lower cholesterol levels via the competitive inhibition of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). In addition, the pleiotropic anti-inflammatory effects of statins on T cells make them attractive as therapeutic drugs in T-cell-driven autoimmune disorders. Since statins do not exclusively target HMGCR and thus might have varying effects on different cell types, we generated a new mouse strain allowing for the tissue-specific deletion of HMGCR. Deletion of HMGCR expression in T cells led to a severe decrease in their numbers with the remaining cells displaying an activated phenotype, with an increased pro…

0301 basic medicineCancer ResearchGeranylgeranyl pyrophosphateCell SurvivalT cellT-LymphocytesImmunologyProtein PrenylationMevalonic AcidCell CountMevalonic acidLymphocyte ActivationT-Lymphocytes Regulatory03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinePolyisoprenyl PhosphatesmedicineAnimalsbiologyCell DeathIntegrasesCholesterolCell BiologyHydroxymethylglutaryl-CoA reductaseCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurePhenotypeBiochemistrychemistryHMG-CoA reductasebiology.proteinProtein prenylationlipids (amino acids peptides and proteins)Hydroxymethylglutaryl CoA ReductasesOriginal ArticleMevalonate pathway030217 neurology & neurosurgeryGene DeletionCell deathdisease
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Lipid-altering efficacy of ezetimibe/simvastatin 10/20 mg compared with rosuvastatin 10 mg in high-risk hypercholesterolaemic patients inadequately c…

2009

SUMMARY Aims: To evaluate the efficacy of switching from a previous statin monotherapy to ezetimibe ⁄simvastatin (EZE ⁄SIMVA) 10 ⁄20 mg vs. rosuvastatin (ROSUVA) 10 mg. Methods: In this randomised, double-blind study, 618 patients with documented hypercholesterolaemia [low-density lipoprotein cholesterol (LDL-C) ‡ 2.59 and £ 4.92 mmol ⁄l] and with high cardiovascular risk who were taking a stable daily dose of one of several statin medications for ‡ 6 weeks prior to the study randomisation visit entered a 6-week open-label stabilisation ⁄screening period during which they continued to receive their prestudy statin dose. Following stratification by study site and statin dose ⁄potency, patien…

AdultMaleSimvastatinmedicine.medical_specialtyimvastatinStatinmedicine.drug_classHypercholesterolemiaCoronary Artery DiseaseGastroenterologyhypercholesterolaemicchemistry.chemical_compoundDouble-Blind MethodEzetimibeRisk FactorsInternal medicinemedicineHumansRosuvastatinRosuvastatin CalciumAgedAged 80 and overSulfonamidesbiologybusiness.industryCholesterolCholesterol LDLGeneral MedicineMiddle AgedFluorobenzenesRosuvastatin CalciumPyrimidinesTreatment OutcomeEndocrinologychemistrySimvastatinHMG-CoA reductasebiology.proteinAzetidinesDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)Ezetimibe/simvastatinHydroxymethylglutaryl-CoA Reductase Inhibitorsbusinessezetimibemedicine.drugInternational Journal of Clinical Practice
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Loss of the preconditioning effect of rosuvastatin during sustained therapy: a human in vivo study

2011

Studies have demonstrated that the acute administration of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors has protective effects in the setting of ischemia-reperfusion (IR). Previously, we demonstrated that a single dose of rosuvastatin prevented IR-induced endothelial dysfunction in humans through a cyclooxygenase-2-dependent mechanism. Whether the chronic administration of HMG-CoA reductase inhibitors provides similar protection remains controversial and is unknown in humans. Eighteen male volunteers were randomized to receive a single dose of rosuvastatin (20 mg) or placebo. Twenty-four hours later, endothelium-dependent, radial artery flow-mediated dilation (FMD) w…

AdultMaleTime FactorsAdolescentEndotheliumPhysiologyCoenzyme AHyperemiaPharmacologyReductaseDrug Administration ScheduleYoung Adultchemistry.chemical_compoundDouble-Blind MethodIschemiaIn vivoPhysiology (medical)medicineHumansRosuvastatinRosuvastatin CalciumOntarioAnalysis of VarianceSulfonamidesCyclooxygenase 2 Inhibitorsbiologybusiness.industryFluorobenzenesVasodilationRosuvastatin CalciumPyrimidinesmedicine.anatomical_structurechemistryCelecoxibRegional Blood FlowReperfusion InjuryRadial ArteryHMG-CoA reductasebiology.proteinCelecoxibPyrazolesHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicinebusinessBlood Flow Velocitymedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
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Subcutaneous gonadotropin therapy in male patients with hypogonadotropic hypogonadism

1991

Objective The response to subcutaneous (SC) gonadotropin replacement therapy, using human chorionic gonadotropin (hCG) and human menopausal gonadotropin (hMG) or hCG alone, was evaluated in male hypothalamic hypogonadism. Design Sixteen patients with hypothalamic hypogonadism were treated with gonadotropins for induction of puberty and normalization of spermatogenesis. The results were analyzed retrospectively. Setting The study was carried out in a clinical endocrinology department providing tertiary care and in private practices of endocrinology. Patients Eight patients with idiopathic hypogonadotropic hypogonadism and eight patients with Kallmann's syndrome in prepubertal or early pubert…

AdultMaleendocrine systemmedicine.medical_specialtyMenotropinsAdolescentmedicine.drug_classmedicine.medical_treatmentChorionic GonadotropinInjections IntramuscularHuman chorionic gonadotropinSemen qualityHypogonadotropic hypogonadismInternal medicineTestisHumansMedicineEunuchismTestosteroneSexual MaturationSpermatogenesisRetrospective StudiesChemotherapybiologyurogenital systembusiness.industryHypogonadismObstetrics and Gynecologymedicine.diseaseSpermEndocrinologyReproductive MedicineHMG-CoA reductasebiology.proteinDrug Therapy CombinationGonadotropinbusinessSpermatogenesisFertility and Sterility
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Coadministration of atorvastatin prevents nitroglycerin-induced endothelial dysfunction and nitrate tolerance in healthy humans.

2010

Objectives We aimed to assess whether concurrent administration of atorvastatin would modify the development of tolerance and endothelial dysfunction associated with sustained nitroglycerin (GTN) therapy in humans. Background Animal studies have demonstrated that administration of 3-hydroxy-3 methylglutaryl coenzyme A reductase inhibitors can protect against GTN-induced endothelial dysfunction and tolerance, likely through an antioxidant mechanism. Methods Thirty-six healthy male volunteers were randomized to receive continuous transdermal GTN (0.6 mg/h) and placebo, atorvastatin (80 mg/day) alone, or continuous transdermal GTN (0.6 mg/h) with concurrent atorvastatin (80 mg/day), all for 7 …

AdultMalemedicine.medical_specialtyEndotheliumendotheliumAdolescentBrachial Arterymedicine.medical_treatmentAtorvastatinVasodilator AgentsBlood PressurePlaceboNitroglycerinYoung AdultDouble-Blind MethodHeart RateReference ValuesInternal medicinemedicineAtorvastatinHumansPyrrolesEndothelial dysfunctionSalinetolerancebiologybusiness.industryDrug Administration RoutesDrug Tolerancemedicine.diseaseVasodilationOxidative StressBlood pressuremedicine.anatomical_structureEndocrinologyHeptanoic AcidsCirculatory systemHMG-CoA reductasebiology.proteincardiovascular systemlipids (amino acids peptides and proteins)Endothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular Medicinebusinessmedicine.drugcirculatory and respiratory physiologyJournal of the American College of Cardiology
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Cholesterol in Alzheimer’s Disease and other Amyloidogenic Disorders

2010

The complex association of cholesterol metabolism and Alzheimer’s disease is presented in depth, including the possible benefits to be gained from cholesterol-lowering statin therapy. Then follows a survey of the role of neuronal membrane cholesterol in Aβ pore formation and Aβ fibrillogenesis, together with the link with membrane raft domains and gangliosides. The contribution of structural studies to Aβ fibrillogenesis, using TEM and AFM, is given some emphasis. The role of apolipoprotein E and its isoforms, in particular ApoE4, in cholesterol and Aβ binding is presented, in relation to genetic risk factors for Alzheimer’s disease. Increasing evidence suggests that cholesterol oxidation p…

Apolipoprotein Emedicine.medical_specialtyStatinbiologyCholesterolmedicine.drug_classMembrane raftFibrillogenesisDiseasechemistry.chemical_compoundEndocrinologychemistryBiochemistryInternal medicineHMG-CoA reductasemedicinebiology.proteinlipids (amino acids peptides and proteins)Cholesterol metabolism
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Lovastatin protects human endothelial cells from killing by ionizing radiation without impairing induction and repair of DNA double-strand breaks.

2006

Abstract Purpose: 3-hydroxy-3-methylglutaryl CoA reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they are reported to exert pleiotropic effects on cellular stress responses, proliferation, and apoptosis. Whether statins affect the sensitivity of primary human cells to ionizing radiation (IR) is still unknown. The present study aims at answering this question. Experimental Design: The effect of lovastatin on IR-provoked cytotoxicity was analyzed in primary human umbilical vein endothelial cells (HUVEC). To this end, cell viability, proliferation, and apoptosis as well as DNA damage–related stress responses were investigated. Results: The data show that lova…

Cancer ResearchProgrammed cell deathDNA RepairDNA repairDNA damageCell SurvivalApoptosisRadioresistanceRadiation Ionizingpolycyclic compoundsmedicineHumansLovastatinCells CulturedCell Proliferationbiologynutritional and metabolic diseasesEndothelial CellsDose-Response Relationship RadiationDNAMolecular biologyEndothelial stem cellOncologyApoptosisCytoprotectionHMG-CoA reductasebiology.proteinCancer researchlipids (amino acids peptides and proteins)Lovastatinmedicine.drugDNA DamageClinical cancer research : an official journal of the American Association for Cancer Research
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The HMG-CoA reductase inhibitor lovastatin protects cells from the antineoplastic drugs doxorubicin and etoposide

2002

Ras-homologous GTPases are involved in the regulation of genotoxic stress-induced gene expression and cell death. Since they need C-terminal isoprenylation for correct intracellular localization and function, we investigated whether depletion of cells from isopren precursor moieties using the HMG-CoA reductase inhibitor lovastatin affects cellular sensitivity to DNA damaging drugs. Here we show that lovastatin renders cells highly resistant to the tumor-therapeutic compound doxorubicin. Desensitization by lovastatin was reverted by co-treatment with GGPP indicating that inhibition of protein geranylgeranylation is involved in acquired doxorubicin resistance. Lovastatin does not influence ce…

CisplatinStatinbiologymedicine.drug_classTopoisomerasenutritional and metabolic diseasesGeneral MedicinePharmacologyHMG-CoA reductasepolycyclic compoundsGeneticsmedicinebiology.proteinCancer researchDNA fragmentationlipids (amino acids peptides and proteins)DoxorubicinLovastatinEtoposidemedicine.drugInternational Journal of Molecular Medicine
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Potential use of HMG-CoA reductase inhibitors (statins) as radioprotective agents

2011

HMG-CoA reductase inhibitors (statins) are widely used in the therapy of hypercholesterolemia. Apart from their lipid-lowering activity, they have pleiotropic effects that are attributed to the inhibition of regulatory proteins, including Ras-homologous (Rho) GTPases. Here, we discuss the potential usefulness of statins to prevent normal tissue damage provoked by radiotherapy. Statins reduce the mRNA expression of pro-inflammatory and pro-fibrotic cytokines stimulated by ionizing radiation in vitro and alleviate IR-induced inflammation and fibrosis in vivo. The currently available data indicate that statins accelerate the rapid repair of DNA double-strand breaks and, moreover, mitigate the …

DNA RepairRadiotherapybiologyRadioprotective AgentDNA repairDNA damagemedicine.medical_treatmentnutritional and metabolic diseasesRadiation-Protective AgentsInflammationGeneral MedicinePharmacologyReductaseCytokineBiochemistryIn vivoHMG-CoA reductasebiology.proteinmedicineHumanslipids (amino acids peptides and proteins)Hydroxymethylglutaryl-CoA Reductase Inhibitorsmedicine.symptomRadiation InjuriesDNA DamageBritish Medical Bulletin
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Lovastatin protects human endothelial cells from the genotoxic and cytotoxic effects of the anticancer drugs doxorubicin and etoposide

2006

Background and purpose: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they exert pleiotropic effects on cellular stress responses and death. Here, we analysed whether lovastatin affects the sensitivity of primary human endothelial cells (HUVEC) to the anticancer drug doxorubicin. Experimental approach: We investigated whether pretreatment of HUVEC with low dose of lovastatin influences the cellular sensitivity to doxorubicin. To this end, cell viability, proliferation and apoptosis as well as DNA damage-triggered stress response were analysed. Key results: Lovastatin reduced the cytotoxic potency of doxorub…

DNA ReplicationCell SurvivalDNA damageApoptosisBiologyPharmacologypolycyclic compoundsmedicineHumansTopoisomerase II InhibitorsDoxorubicinLovastatinEtoposideEtoposideFluorescent DyesPharmacologyAntibiotics AntineoplasticReverse Transcriptase Polymerase Chain ReactionTopoisomeraseCell CycleEndothelial Cellsnutritional and metabolic diseasesAntimutagenic AgentsFibroblastsCell cycleResearch PapersAntineoplastic Agents PhytogenicDoxorubicinDrug Resistance NeoplasmHMG-CoA reductasebiology.proteinlipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsTopoisomerase-II InhibitorReactive Oxygen SpeciesFluorescein-5-isothiocyanateDNA Damagemedicine.drugBritish Journal of Pharmacology
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